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  • 1
    Electronic Resource
    Electronic Resource
    Circadian Blood Pressure Variation Related to Morbidity and Mortality from Cerebrovascular and Cardiovascular Diseases (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 783 (1996), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1996.tb26715.x
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  • 2
    Electronic Resource
    Electronic Resource
    DO KININS MEDIATE CARDIOPROTECTIVE AND RENOPROTECTIVE EFFECTS OF CILAZAPRIL IN SPONTANEOUSLY HYPERTENSIVE RATS WITH RENAL ABLATION? (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 22 (1995), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. We assessed the potential of the kallikrein–-kinin system in mediating the cardioprotective and renoprotective effects of an angiotensin-converting enzyme inhibitor (ACEI), cilazapril (CIL) in rats with renal ablation.2. Eight week old spontaneously hypertensive rats (SHR) were subjected to 5/6 nephrectomy. One week after the operation, the rats were divided into 5 groups: (i) vehicle; (ii) CIL 1 mg/kg per day per os (p.o.); (iii) Hoe140 (HOE) 70 μg/kg per day given intraperitoneally (i.p.); (iv) CIL 1 mg/kg per day p.0. plus HOE 7 7μg/kg per day i.p.; (v) CIL 1 mg/kg per day p.o. plus HOE 70 μg/kg per day i.p. The treatment lasted for 4 weeks.3. CIL alone significantly reduced systolic blood pressure, urinary protein excretion, heart weight and serum creatinine level. HOE alone did not induce any significant changes in these parameters. CIL in combination with HOE (7 or 70 μg/kg per day) did not induce any changes in these parameters, in addition to those associated with the effects of CIL alone.4. These results indicate that the kallikrein-kinin system might not play a major role in the cardioprotective and renoprotective effects of ACE inhibitors in the rat remnant kidney model of chronic renal failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1995.tb02953.x
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  • 3
    Electronic Resource
    Electronic Resource
    CARDIOVASCULAR AND RENAL PROTECTIVE EFFECTS OF LOSARTAN IN SPONTANEOUSLY HYPERTENSIVE RATS WITH DIABETES MELLITUS (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 22 (1995), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Cardiovascular and renal benefits of a specific angiotensin II (AII) receptor antagonist, losartan (LOS), were assessed in diabetic rats with renal impairment.2. Uninephrectomized SHR made diabetic by streptozotocin administration were given LOS (5 mg/kg per day, i.p.) alone, captopril (CAP) (50 mg/kg per day, i.p.) alone, or a combination of CAP and LOS via osmotic minipumps for 8 weeks.3. Both CAP alone and LOS alone completely blocked the development of hypertension in diabetic SHR in the same manner. CAP + LOS did not enhance the antihypertensive effects of LOS alone or CAP alone.4. CAP+LOS, LOS alone and CAP alone significantly decreased urinary protein excretion and serum creatinine to the same extent.5. These results indicate that both LOS and CAP exert antihypertensive and renoprotective effects in this model: these actions are mainly through inhibition of AII production.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1995.tb02956.x
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  • 4
    Electronic Resource
    Electronic Resource
    DECREASED CONVERSION OF BIG ENDOTHELIN-1 TO ENDOTHELIN-1 IN PATIENTS WITH DIABETES MELLITUS (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 18 (1991), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1991.tb01388.x
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  • 5
    Electronic Resource
    Electronic Resource
    Combination of vasopressin and angiotensin inhibition in experimental focal glomerulosclerosis (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Nephrology 3 (1997), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary: This study was designed to investigate the role of vasopressin and angiotensin II in the pathogenesis of focal glomerulosclerosis (FGS). A non-peptide vasopressin VI antagonist (OPC-21268) and an angiotensin converting enzyme inhibitor (ACE-I) were administered either alone or in combination for 15 weeks to FGS, spontaneously hypercholesterolaemic rats. Treatment with the V1 antagonist (1% OPC-21268) suppressed the rise in systolic blood pressure (SBP), serum triglyceride (TG), blood urea nitrogen (BUN) and serum creatinine (S-Cr) levels, but not the elevations of urinary protein excretion (UPE) or serum total cholesterol (TC) levels. Morphologically, V1 antagonist significantly prevented an increase in the index of glomerular sclerosis (IS) and relative interstitial volume (RIV). In the low dose/high dose of V1 antagonist supplementation, the administration of 0.2% OPC-21268 failed to suppress any increase in the SBP and TG levels, but significantly preserved renal function and attenuated renal lesions. In the combination study, rats were divided into four groups: (i) V1 antagonist (1% OPC-21268); (ii) ACEI (imidapril, 5 mg/kg/per day); (iii) both treated groups; and (iv) an untreated control group. Angiotensin-converting enzyme inhibitor significantly suppressed increases in SBP, UPE, TC, BUN, and S-Cr levels compared with V1 antagonist. the combination therapy significantly enhanced these effects. Both agents significantly reduced IS and RIV, and combination therapy further reduced these levels. the results indicated that vasopressin, as well as angiotensin II, via the V1 receptor cause hypertension and renal injury in FGS rats. Vi antagonist and ACE-I have antihypertensive and renoprotective effects in this FGS model, and enhanced their beneficial effects when used as combination therapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1797.1997.tb00255.x
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  • 6
    Electronic Resource
    Electronic Resource
    ROLE OF NITRIC OXIDE IN THE CONTROL OF GLOMERULAR MICROCIRCULATINO (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 24 (1997), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Nitric oxide (NO) plays an important role in the control of glomerular haemodynamics and is synthesized from the amino acid L-arginine by a family of enzymes, NO synthase (NOS).2. Nitric oxide synthase is present in the endothelium and also in the macula densa, a plaque of specialized tubular epithelial cells. Endothelial NOS is known to be stimulated by shear stress and hormones, while the factor that regulates the activity of macula densa NOS remains undefined.3. Studies with the in vitro microperfusion of glomerular arterioles have shown that the constriction of afferent arterioles (Af-Art) induced by myogenic responses and angiotensin II (AngII) is stronger in the absence rather than in the presence of luminal flow. Furthermore, endothelial disruption or NOS inhibition abolishes such differences, suggesting that flow through the lumen stimulates the endothelium to synthesize and release NO, which in turn attenuates both the myogenic response and the action of AngII in the Af-Art.4. In contrast, NOS inhibitors have no effect on efferent arteriolar (Ef-Art) constriction induced by AngII.5. In preparations in which Af-Art and the macula densa are simultaneously microperfused, selective inhibition of macula densa NOS has been shown to augment Af-Art constriction when the NaCl concentration at the macula densa is high, suggesting that the macula densa produces NO, which in turn modulates tubuloglomerular feedback.6. Thus, the differential actions of NO in the Af-Art, Ef-Art and the macula densa may be important in the control of glomerular haemodynamics under various physiological and pathological conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1997.tb02094.x
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  • 7
    Electronic Resource
    Electronic Resource
    CONTRACTILE PROPERTIES OF AFFERENT AND EFFERENT ARTERIOLES (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 24 (1997), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The balance of vascular tone of the afferent and efferent arteriole is a crucial determinant of glomerular haemodynamics. Despite their intimate anatomical relationship in the juxtaglomerular apparatus, the mechanisms that regulate afferent and efferent arteriolar tone are different.2. In the afferent arteriole, two intrinsic mechanisms, the myogenic response and macula densa-mediated tubuloglo-merular feedback (TGF) play a dominant role, maintaining the glomerular filtration rate (GFR) at a constant level over a wide range of renal perfusion pressure. Studies have shown that these two mechanisms are modulated by nitric oxide (NO). In addition, an interaction between TGF and angiotensin II (AngII) seems to be essential to maintaining GFR despite large variations in daily intake of salt and water.3. In the efferent arteriole, neither myogenic response nor TGF seems to be important, while AngII is one major factor involved in the control of vascular resistance. In addition, recent studies have provided evidence that NO and prostaglandins produced by the glomerulus may control resistance of the downstream efferent arteriole.4. As the early segment of the efferent arteriole resides within the glomerulus, various autacoid hormones produced by the glomerulus may reach and directly act on this segment, thereby controlling the glomerular capillary pressure. Thus, it would be important to understand the differences in the mechanisms operating at the afferent and efferent arteriole, as well as their alterations in various physiological and pathological conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1997.tb01241.x
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  • 8
    Electronic Resource
    Electronic Resource
    Contribution of cellular infiltration to the progression of IgA nephropathy: A longitudinal, immunocytochemical study on repeated renal biopsy specimens (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Nephrology 1 (1995), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary: A retrospective immunocytochemical study was performed on repeated renal biopsy specimens from 47 patients with IgA nephropathy, 23 of whom received steroid therapy after the initial biopsy. Immune cells in renal tissues were detected by the immunoperoxidase method using monoclonal antibodies against common leukocyte antigens, T cells, B cells and monocytes/macrophages.Overall, glomerular infiltration of total leukocytes and monocytes/macrophages was significantly correlated with proteinuria. Interstitial infiltration of total leukocytes, T cells and monocytes/macrophages was significantly correlated with histological injury and renal dysfunction. In the steroid-treated group (group S), urinary protein and glomerular infiltration of total leukocytes and macrophages were significantly reduced at the follow-up biopsy, while these parameters remained unchanged in the nonsteroid-treated group (group N). In group S, interstitial infiltration of almost all of the various cell types, histological renal damage and renal function remained unchanged at the follow-up biopsy, while group N showed a significant increase in the number of interstitial total leukocytes, T cells and macrophages and showed a significant progression of histological renal injury.These findings suggest that glomerular immune cells, especially monocytes/macrophages, are involved in inducing proteinuria and interstitial immune cells are involved in renal deterioration. Furthermore, steroid therapy appears to reduce urinary protein and prevent the progression of tissue injury through suppression of renal infiltration of these inflammatory cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1797.1995.tb00019.x
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  • 9
    Electronic Resource
    Electronic Resource
    EFFECTS OF RECOMBINANT HUMAN ERYTHROPOIETIN ON BLOOD PRESSURE AND RENAL FUNCTION IN SHR WITH CHRONIC RENAL FAILURE (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 22 (1995), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The effects of chronic administration of erythropoietin (EPO) on blood pressure and renal function in rats with ablation of renal mass were assessed.2. Spontaneously hypertensive rat were subjected to 5/6 nephrectomy (5/6Nx). Four weeks after the operation, the rats were randomly allocated to vehicle, EPO 20 IU/kg i.p., or EPO 100 W/kg i.p. (both given twice a week) for 4 weeks.3. Marked anaemia was noted in SHR-5/6Nx. EPO caused a significant increase in haematocrit at a high dose but not at a low dose. A dose dependent relationship was noted in the EPO-induced rise in the systolic blood pressure.4. EPO dose-dependently increased urinary protein excretion. It also increased blood urea nitrogen and serum creatinine levels.5. These results suggest that EPO ameliorates anaemia and severely accelerates renal failure in SHR-5/6Nx. They also suggest that anaemia can be a haemodynamieally favourable adaptation to chronic renal disease and that its correction may have adverse renal haemodynamic and structural consequences.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1995.tb02865.x
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  • 10
    Electronic Resource
    Electronic Resource
    EFFECTS OF ISOTONIC SALINE LOADING ON RENAL TUBULAR AND NEUROGENIC DOPAMINE RELEASE IN CONSCIOUS RABBITS (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 22 (1995), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. This study was designed to investigate the effects of isotonic saline loading on renal tubular and neurogenic dopamine (DA) in conscious rabbits.2. Isotonic saline loading did not affect mean arterial pressure, heart rate or renal blood flow but markedly increased urine volume, sodium excretion and DA excretion.3. Renal DA spillover was not affected by venous emptying, while renal noradrenaline (NA) spillover tended to decrease during saline loading. The ratio of % renal DA spillover to % renal NA spillover increased to 2.3 ± 0.6 (P 〈 0.05) 3h after saline loading.4. Isotonic saline loading increased renal tubular DA production but had little effect on neurogenic DA release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1995.tb02047.x
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